Bihler I, Sawh P C
Mol Cell Endocrinol. 1980 Jul;19(1):93-100. doi: 10.1016/0303-7207(80)90033-7.
The role of external Ca2+ in the regulation of sugar transport in isolated resting atria of rats and guinea pigs was studied by measuring the tissue/medium distribution of 14C-labelled 3-methylglucose and of 45Ca. Omission of Ca2+ from the medium strongly antagonized the stimulation of sugar transport by insulin, hyperosmolarity (100 mM mannitol) or Na+-pump inhibition (K+-free medium). Basal sugar transport was not affected by Ca2+ omission but was increased when 0.5 mM EGTA was also added. The Ca2+ antagonist drug D-600 decreased 45Ca influx and also inhibited sugar-transport stimulation by the above 3 treatments in the rat, while in the guinea pig it antagonized only insulin-stimulated transport. The stimulation of sugar transport by a high adrenaline concentration and the inhibition by a low concentration were both antagonized by Ca2+ omission or D-600. The results illustrate the important role of Ca2+ influx in the control of sugar transport by hormonal and other modulators and are consistent with the hypothesis that cytoplasmic Ca2+ regulates glucose transport in muscle.
通过测量¹⁴C标记的3-甲基葡萄糖和⁴⁵Ca在组织/培养基中的分布，研究了细胞外Ca²⁺在大鼠和豚鼠离体静息心房糖转运调节中的作用。培养基中去除Ca²⁺强烈拮抗胰岛素、高渗（100 mM甘露醇）或钠泵抑制（无钾培养基）对糖转运的刺激作用。基础糖转运不受去除Ca²⁺的影响，但当加入0.5 mM乙二醇双四乙酸（EGTA）时会增加。Ca²⁺拮抗剂药物D-600减少了⁴⁵Ca内流，并且在大鼠中也抑制了上述三种处理对糖转运的刺激作用，而在豚鼠中它仅拮抗胰岛素刺激的转运。高浓度肾上腺素对糖转运的刺激作用和低浓度肾上腺素的抑制作用均被去除Ca²⁺或D-600所拮抗。这些结果说明了Ca²⁺内流在激素和其他调节剂对糖转运控制中的重要作用，并且与细胞质Ca²⁺调节肌肉中葡萄糖转运的假说一致。
